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PubMed1987

Reserpine increases chromaffin cell enkephalin stores without a concomitant decrease in other proenkephalin-derived peptides.

Reserpine increases the levels of enkephalins in adrenal medullary chromaffin cells; however, the origin of the newly apparent pentapeptides has been the subject of debate, because no increase in the levels of proenkephalin mRNA has been observed. The present study was performed for determining if the reserpine-induced increase in context of enkephalins was derived from processing of preexisting fragments of proenkephalin. Bovine chromaffin cell enkephalins and larger enkephalin-containing peptides were separated by reversed-phase HPLC and identified by approximate molecular weight, elution with peptide standards, and enkephalin sequences contained. Treatment of the cells with reserpine increased the levels of enkephalins and of enkephalin-containing peptides of up to approximately 3 kilo-daltons without reducing the levels of larger enkephalin-containing peptides. Similar results were obtained with another catecholamine-depleting drug, tetrabenazine. In contrast, treatment of chromaffin cells with theophylline or forskolin increased the levels of both enkephalins and enkephalin-containing peptides of all sizes. The results suggest that new synthesis of proenkephalin is required for the effects of reserpine, although proenkephalin processing is also altered by this drug.

Adrenal Glands↗
PubMed1988

Long-term changes in rat brain tyrosine hydroxylase following reserpine treatment: a quantitative immunochemical analysis.

An immunoblot procedure was developed to quantify the amount of tyrosine hydroxylase protein in homogenate of small brain regions. With the use of this method we have studied the variations in tyrosine hydroxylase activity and protein levels in some catecholaminergic neurons at different times following a single reserpine injection (10 mg/kg s.c.) and reevaluated the anatomical specificity of tyrosine hydroxylase induction by this drug. Reserpine administration provoked a long-lasting increase in both tyrosine hydroxylase activity and protein levels within locus ceruleus neurons. This effect culminated at day 4 after injection. At this time, the enzyme activity and protein levels in treated animals were respectively 2.7 and 2.6 times that measured in vehicle-treated animals. Both parameters varied in parallel so that tyrosine hydroxylase specific activity did not change over time. In contrast, reserpine did not cause any changes in tyrosine hydroxylase activity in the dopaminergic neurons of the substantia nigra, but provoked a moderate increase in tyrosine hydroxylase protein level. This latter effect was maximal (1.5 times) 4 days after treatment. In the adjacent dopaminergic area, i.e., the ventral tegmental area, a small decrease in the enzyme activity was recorded at day 2 without any significant change in the level of the protein. In conclusion, first, our data show the capacity of our method to assay tyrosine hydroxylase protein amounts in small brain catecholaminergic nuclei. Second, our results confirm and extend previous studies on the effect of reserpine on the regulation of tyrosine hydroxylase level within brain noradrenergic neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1992

Different natures of supersensitivity of adenylate cyclase stimulated by calcitonin gene-related peptide and isoproterenol in rat diaphragm after denervation and reserpine treatment.

In skeletal muscles, calcitonin gene-related peptide (CGRP) released from motor nerve terminals and humoral catecholamines stimulate adenylate cyclase (AC) and enhance muscle contraction. The effects of denervation and treatment with reserpine on twitch contraction and the AC system in rat diaphragm were investigated. The basal levels of twitch contraction and AC activity of the diaphragm of rats were both increased 2 weeks after phrenic nerve denervation but were not altered by treatment with reserpine. Reserpine treatment provoked supersensitivity of AC to isoproterenol, without affecting the response to CGRP. On the other hand, denervation decreased the activation of AC and enhancement of twitch contraction by CGRP, without affecting the responses to isoproterenol. These data suggest that denervation causes up-regulation of AC as a result of loss of CGRP release from nerve terminal and that depletion of catecholamines by reserpine treatment supersensitizes the responses at the beta-adrenoceptor level. Thus, nervous and humoral factors regulate the AC system in striated muscle by different mechanisms.

Adenylyl Cyclases↗
PubMed1982

Characterization of the adrenoreceptor activities of isoprenaline in the field stimulated rat vas deferens: selective supersensitivity to beta 2-mediated responses following reserpine treatment.

1 Low concentrations of isoprenaline (EC50 = 45.6 nM) inhibited contractions in the isolated field stimulated rat vas deferens. This inhibitory effect was markedly attenuated by the postjunctional beta 2-adrenoreceptor antagonist timolol, but not affected by the prejunctional alpha 2 or postjunctional alpha 1-adrenoreceptor antagonists rauwolscine and prazosin, respectively. 2 In vas deferens of rats previously treated with reserpine, the postjunctional beta 2-adrenoreceptor-mediated inhibitory response to isoprenaline was markedly potentiated. 3 High concentrations of isoprenaline (EC50 = 1.5 microM) also inhibited contractility in tissues in which postjunctional beta 2-adrenoreceptors were maximally blocked by high concentrations of timolol. This contractile inhibition produced by isoprenaline was abolished by rauwolscine but not significantly altered by prazosin or pretreatment of the rats with reserpine indicating stimulation of prejunctional alpha 2-adrenoreceptors. 4 Rauwolscine pretreatment unmasked an ability of isoprenaline (EC50 = 17.1 microM) to produce enhancement of field stimulation-induced contractions. This response was abolished by prazosin but was unaffected by timolol or reserpinization indicating an action upon postjunctional alpha 1-adrenoreceptors. 5 The data indicate isoprenaline activates adrenoreceptor mechanisms in the field stimulated rat vas deferens by a direct action not dependent upon endogenous catecholamines and with an order of activity of beta 2 much greater than alpha 2 greater than alpha 1. Pretreatment with reserpine produces rapid and selective development of supersensitivity to the postjunctional beta 2-mediated inhibitory response of isoprenaline in this preparation.

Animals↗
PubMed1957

Metabolic and other effects of reserpine upon smooth and skeletal muscle.

Reserpine increased the concentration of potassium ions in the fluid bathing the isolated frog sartorius muscle. The effect of reserpine upon respiration and upon glycolysis in rabbit intestinal muscle has been investigated using the Warburg "Direct" method. After a latent period, reserpine (50 mug./ml.) depressed respiration but did not affect glycolysis in gut muscle. These results, together with previous observations, may point to an effect of reserpine upon carbohydrate metabolism.

Animals↗
PubMed1958

The action of sympathomimetic amines on heart rate in relation to the effect of reserpine.

When the heart-lung preparation is made from a dog treated with reserpine, catechol amines such as noradrenaline and isoprenaline have a greater effect on the rate of the heart than they have in a preparation from a normal dog. Other sympathomimetic amines such as tyramine and ephedrine, on the other hand, are found to have lost their action. Since treatment with reserpine has been shown to cause the store of noradrenaline in the heart to disappear, and the infusion of noradrenaline into the preparation made from a reserpine-treated animal restores the action of tyramine, it is concluded that substances like tyramine and ephedrine normally act by liberating noradrenaline from the store, and do not act directly. Cocaine, like reserpine, increases the effect of noradrenaline and decreases the effect of tyramine on the heart rate; it appears to block the release of noradrenaline from the store in the heart.

Amines↗
PubMed1960

Interaction between histamine and dichloroisoproterenol, hexamethonium, pempidine, and diphenhydramine, in normal and reserpine-treated heart preparations.

Histamine stimulated the isolated auricles and heart of the guinea-pig. The effect was best seen in auricles which had been previously depressed by treatment with reserpine. Ganglionic blocking drugs (hexamethonium and pempidine), applied to auricles which had been previously treated with reserpine, abolished the diphasic effect of nicotine, but did not alter the response to histamine. Dichloroisoproterenol did not modify the stimulant action of histamine in isolated auricles, either before or after treatment with reserpine; nor did it alter the response of the isolated heart. Diphenhydramine reduced or blocked the stimulant action of histamine in auricles which had been previously treated with reserpine. The results support the hypothesis that histamine stimulates the myocardium by a direct action on specific receptors.

Diphenhydramine↗
PubMed1961

Effect of reserpine on growth and sexual development of chickens.

One-month-old male chickens were given injections of 1 mg, 2 mg and 4 mg/kg of reserpine. The injections were repeated at weekly intervals for three months. The chickens receiving reserpine grew at half the rate of untreated control chickens and failed to grow combs. At 4 months of age the testes of reserpine-treated chickens were only about one-tenth the weight of the testes of the control chickens and histologically they showed extreme hypoplasia of the seminiferous tubules. Two large doses of reserpine one month apart could cause atrophy of the testes of adult roosters.

Animals↗
PubMed1962

Effect of reserpine on the acetylcholine content of the heart, the ileum and the hypothalamus of the dog.

The effect of intravenous administration of reserpine in 10 dogs was studied on the acetylcholine content of the sino-atrial node, the right auricle and the right ventricle of the heart, the ileum and the hypothalamus of dog. The general sedation, the bradycardia, and the purgative effects of reserpine were also noted. Tissues were removed for estimation of acetylcholine when bradycardia was maximal. Reserpine increased the acetylcholine content of all the tissues studied. The increase in the peripheral tissues was greater than in the hypothalamus. The bradycardia and the purgative effects of reserpine may be related to the increase of the acetylcholine content of the sino-atrial node and the ileum.

Acetylcholine↗
PubMed1968

Antagonism of reserpine-induced emesis in pigeons: a screening method for antidepressant activity.

1. Various antidepressant drugs and procedures have been studied against reserpine-induced emesis in pigeons.2. Electroconvulsions, pentylenetetrazol and a non-hydrazide monoamine oxidase inhibitor (pargyline) block reserpine emesis.3. It is suggested that reserpine-induced emesis in pigeons provides a simple and reliable method for studying anti-reserpine activity, and the compounds effective in antagonizing this emetic response are likely to have antidepressant property.

Animals↗
PubMed1970

Nonspecific supersensitivity of the guinea-pig vas deferens produced by decentralization and reserpine treatment.

1. The sensitivity of the guinea-pig vas deferens to noradrenaline, histamine, methylfurmethide and potassium was examined in vitro following decentralization and reserpine treatment.2. One day after decentralization or administration of reserpine (1.0 mg/kg daily) the sensitivity of the vas deferens was not increased. After 5 days' treatment the muscle was supersensitive to all four stimulants.3. The magnitude of the sensitivity increase to an individual drug was the same following both chronic reserpine treatment and decentralization. However, the degree of supersensitivity differed for the four stimulants. The order of potentiation was noradrenaline>histamine>methylfurmethide>potassium.4. The magnitude of the supersensitivity was inversely correlated with the slope of the dose-response curves to the four agonists. The dose-response curve to potassium had the steepest slope, followed in order by methylfurmethide, histamine and noradrenaline.5. A hypothesis is presented to account for the inverse relationship between the slope of the dose-response curve and the degree of supersensitivity which follows reserpine treatment or decentralization.

Animals↗
PubMed1972

Effect of sympathomimetic drugs in eliciting hypertensive responses to reserpine in the rat, after pretreatment with monoamineoxidase inhibitors.

1. The effects of some rapidly metabolized sympathomimetic amines, such as beta-phenylethylamine and p-tyramine, in eliciting hypertensive responses to reserpine in the anaesthetized rat, have been studied.2. Retardation of metabolism, by pretreatment with the monoamineoxidase inhibitors iproniazid or phenelzine, causes beta-phenylethylamine (which in untreated rats has no effect) to induce hypertensive responses to reserpine. Tyramine and other hydroxy substituted phenylethylamines are much less active in this respect, probably because of relatively poor lipid solubility.3. Hypertensive responses to reserpine are due to catecholamine release, which is believed to be from stores made accessible to indirectly acting sympathomimetic amines with high lipid solubility by an action of reserpine on cell membranes.

Animals↗
PubMed1974

The effect of pithing and of nerve stimulation on the depletion of noradrenaline by reserpine in the rat anococcygeus muscle and vas deferens.

1 The depletion of noradrenaline (NA) in the rat anococcygeus muscle and vas deferens by reserpine and the effect on this of the abolition of nerve activity by pithing and reinforcement of nerve activity by stimulation of the spinal cord outflows has been studied.2 NA depletion of the anococcygeus and vas deferens measured 24 h after reserpine was similar and was related to dose. The heart was depleted faster than the two smooth muscle tissues.3 In the absence of reserpine neither abolition of nerve activity by pithing nor its reinforcement by nerve stimulation had a detectable influence on NA content of the anococcygeus or vas deferens.4 In rats given reserpine (200 mug/kg), increasing nerve activity by spinal stimulation significantly increased NA depletion in both the anococcygeus and the vas deferens when compared with animals pithed but not stimulated. These results confirm that nerve impulse traffic can be an important factor in determining the rate of depletion of NA by reserpine.5 The mechanical response to nerve stimulation in both the vas deferens and anococcygeus was resistant to quite severe depletion of their NA content, with the exception of the initial fast component of the response in the vas. The implications of these results for motor transmission in the vas deferens are discussed.

Anal Canal↗
PubMed1976

The relationship between calcium and increased sensitivity of rabbit aortae four hours after reserpine.

1 Four hours after reserpine, rabbit aortic strips were supersensitive to acetylcholine, isoprenaline and noradrenaline. The threshold concentration of the drugs necessary to induce a response was less and the maximum tension developed by the tissues was greater than in control strips. 2 Reserpine-treatment potentiated the contractile responses to CaCl2. 3 Reserpine-treatment resulted in an increase in calcium uptake and an increase in the slow component of 45Ca2+ efflux. 4 After resperine-treatment, the rate of relaxation from a potassium-induced contraction was decreased. 5 It is concluded that reserpine-induced supersensitivity is related to an enhanced ability of the tissue to retain and utilize calcium.

Acetylcholine↗
PubMed1977

Selective reserpine-induced supersensitivity of the positive inotropic and chronotropic responses to isoprenaline and salbutamol in guinea-pig isolated atria.

1 Dose-response curves for the positive inotropic and chronotropic responses to isoprenaline were obtained in atria from untreated guinea-pigs and those receiving various reserpine pretreatments. 2 Tension responses were unaffected, whereas rate responses were depressed by the lowest dose of reserpine (0.05 mg/kg i.p. at 24 hours). 3 With larger 24 h doses and a 3 day pretreatment, the rate and tension dose-response curves were progressively displaced to the left, indicating supersensitivity which was greater for tension at each pretreatment. 4 No supersensitivity to histamine or Ca2+ could be detected, leading to the conclusion that it was selective for the beta-adrenoceptor agonists possibly at the receptor level. 5 As an indication of the adrenergic neurone depleting effectiveness of each reserpine dosage, preparations were exposed to test doses of beta-phenylethylamine. 6 Salbutamol was a partial agonist in untreated atria, the maximum rate (63.3%) and tension (10.0%) responses being less than those for isoprenaline. In atria from reserpine pretreated animals the supersensitivity was revealed as an increase of this maximum compared with isoprenaline. 7 The significance of this observation in relation to the possible mechanism of the supersensitivity is discussed.

Albuterol↗
PubMed1985

The effect of reserpine treatment on the extraneuronal uptake of [3H]-isoprenaline into rat atria.

Treatment of rats with reserpine (1 mg kg-1 day-1) for up to 7 days resulted in a marked decrease in a corticosterone-sensitive component of the extraneuronal accumulation of [3H]-isoprenaline into their atria. The change in extraneuronal uptake did not appear to be due to a direct action of reserpine on the uptake mechanism, since it was several days before the treatment had a significant effect on the accumulation of [3H]-isoprenaline. Further, reserpine in vitro did not inhibit extraneuronal uptake. The reserpine-induced change in the accumulation of [3H]-isoprenaline was not an artifact due to changes in water balance, ion distribution, extracellular space or tissue atrophy. Nor was the change due to an increase in the efflux of [3H]-isoprenaline from the tissue. These experiments support the suggestion that the extraneuronal uptake is dependent upon a functional adrenergic innervation.

Animals↗
PubMed1989

The effects of acute and chronic desipramine on the thermogenic and hypoactivity responses to alpha 2-agonists in reserpinized and normal mice.

1. The effects of acute and chronic (14 day) administration of the noradrenaline uptake inhibitor, desipramine (DMI), on the thermogenic responses to clonidine in reserpine-treated mice, and on the hypothermic and hypoactivity responses to the alpha 2-agonist, UK-14,304, in untreated mice were examined. 2. Taking the capacity of DMI to delay the onset of reserpine-induced hypothermia as an indicator of noradrenaline (NA) uptake inhibition, the lowest dose of DMI to inhibit uptake significantly for 12 h in the mouse was shown to be between 10 and 20 mg kg-1 orally. 3. Chronic (every 12 h for 14 days), but not acute treatment with DMI (15 mg kg-1, orally), attenuated the thermogenic responses to low doses (0.02-0.225 mg kg-1, i.p.) of clonidine (injected 20 h after the last dose of DMI) in reserpinized mice. 4. Acute DMI administration slightly attenuated the hypothermia and hypoactivity induced by UK-14,304 (0.25-1.0 mg kg-1, i.p.) when injected 2h, but not when injected 18-21h before the agonist. In contrast, 18-21h after withdrawal from chronic DMI both of these responses to UK-14, 304 were markedly attenuated. 5. As the thermogenic response to clonidine in reserpinized mice appears to involve central post-synaptic alpha 2-adrenoceptors, these results suggest that prolonged inhibition of NA uptake decreases the sensitivity of postsynaptic alpha 2-adrenoceptors. The results of the studies using UK-14,304 indicate that central alpha 2-adrenoceptors involved in mediating other behavioural and pharmacological responses to alpha 2-agonists are also down-regulated by chronic inhibition of NA uptake.

Adrenergic alpha-Agonists↗
PubMed1985

Comparison of the use of reserpine versus alpha-methyldopa for second step treatment of hypertension in the elderly.

A retrospective chart analysis was conducted on all new elderly hypertensive patients referred to a community hypertension clinic who were being treated with either reserpine or alpha-methyldopa plus a diuretic. There were no significant differences between the two groups on entry in age, gender, co-morbid diagnoses, or systolic or diastolic blood pressure. There were no significant differences between the two groups in terms of side effects over three years, but the proportion of persons having compliance problems was significantly lower in the reserpine group. Mean diastolic pressures were significantly lower after one, two, and three years, and systolic pressures were lower after one and two years in the reserpine group. Reserpine is at least as effective as alpha-methyldopa in treating hypertension in the elderly and is associated with fewer problems in compliance.

Aged↗